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Fig. 1 | Molecular Medicine

Fig. 1

From: Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects

Fig. 1

Illustration of the hedgehog pathway. Hh: Hedgehog; SMO: Smoothened; PTCH: Patched; SuFu: Suppressor of Fused; Cos 2: Kinesin-like molecule costal 2; Ci: Cubitus interruptus; Fu: Serine/threonine protein kinase Fused. In the absence of the Hh ligand, PTCH receptor suppresses (shown by the dashed line) the G-protein coupled receptor (GPCR) named SMO. Hence, no further signaling cascade takes place which prevents cell proliferation. Hh signaling gets activated when a Hh ligand such as Sonic Hh binds to the PTCH. This ligand binding relieves the SMO, thereby it to modulate a complex known as hedgehog signaling complex (HSC). HSC is comprised of four different proteins namely SuFu, Fu, Cos2, and Ci. Here, in the figure, Ci is not shown in association with HSC. In the absence of Hh ligand, Cos2-Fu-Ci complex interacts with the C-tail of SMO which leads to the active form of Ci (Ci-A) that is responsible for the activation of target genes, leading to cellular processes like cell proliferation, and differentiation. In the absence of the Hh ligand, SuFu-Ci and Cos2-Fu-Ci complexes promote the repressor form of Ci (Ci-R), thereby preventing it to activate the target genes (Jia et al. 2015)

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